The factors that regulate the intestinal blood flow play a vital role in the develpoment of mesenteric ischemia. Mucosa of the intestines has a high metabolic activity and accordingly a high blood flow requirement. The majority of blood supply of the intestine comes from the superior mesenteric artery, with a collateral blood supply from superior and inferior pancreaticoduodenal arteries (branches of the celiac artery) as well as the inferior mesenteric artery. The splanchnic circulation (arteries supplying the viscera) receives 15-35% of the cardiac output, making it sensitive to the effects of decreased perfusion. Mesenteric ischemia occurs when intestinal blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disrutpion of mucosal barrier, allowing the release of bacterial toxins (present in the intestinal lumen) and vasoactive mediators which ultimately lead to complete necrosis (cell death) of the intestinal mucosa. This can further progress to depression in myocardial activity, sepsis, multiorgan failure, and without prompt intervention, even death.<ref name="pmid9146713">{{cite journal| author=Rosenblum JD, Boyle CM, Schwartz LB| title=The mesenteric circulation. Anatomy and physiology. | journal=Surg Clin North Am | year= 1997 | volume= 77 | issue= 2 | pages= 289-306 | pmid=9146713 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9146713 }} </ref>

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The factors that regulate the [[intestinal]] blood flow play a vital role in the development of mesenteric ischemia. [[Mucosa]] of the [[intestines]] has a high metabolic activity and accordingly a high blood flow requirement. The majority of blood supply of the [[intestine]] comes from the [[superior mesenteric artery]], with a collateral blood supply from superior and inferior [[Pancreaticoduodenal artery|pancreaticoduodenal arteries]] (branches of the [[celiac artery]]) as well as the [[inferior mesenteric artery]]. The [[splanchnic]] circulation ([[arteries]] supplying the [[viscera]]) receives 15-35% of the [[cardiac output]], making it sensitive to the effects of decreased [[perfusion]]. Mesenteric ischemia occurs when [[intestinal]] blood supply is compromised by more than 50% of the original blood flow without activation of adaptive responses. This can lead to disruption of [[mucosal]] barrier, allowing the release of [[Bacterial toxin|bacterial toxins]] (present in the [[intestinal]] lumen) and [[vasoactive]] mediators which ultimately lead to complete [[necrosis]] (cell death) of the intestinal mucosa. This can further progress to depression in [[myocardial]] activity, [[sepsis]], [[multiorgan failure]], and without prompt intervention, even death.

* These arteries can compensate for 75% reduction in mesenteric blood flow for upto 12 hours, without substanial injury.

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* [[Intestines]] receive collateral blood supply at all levels from the superior and inferior pancreaticoduodenal arteries, branches of the [[celiac artery]], which provide protection from [[ischemia]].

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* These arteries can compensate for 75% reduction in [[mesenteric]] blood flow for up to 12 hours, without substanial injury.

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* An extensive [[collateral circulation]] protects the [[intestines]] from transient periods of inadequate [[perfusion]]. However, prolonged reduction in [[splanchnic]] blood flow leads to [[vasoconstriction]] in the affected [[vascular bed]], and eventually reduces collateral blood flow.

* The areas lacking this collateralization are prone towards ischemia.

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* [[Vasoactive]] and [[humoral]] factors control the regulation of [[vascular]] tone of [[mesenteric]] circulation in response to periods of stress such as [[systemic hypotension]] or [[postprandial]] state.

* Intrinsic regulatory system that includes metabolic and myogenic factors.

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* Reduction in blood supply to the [[mesentery]] causes adaptive changes in the [[splanchnic]] circulation.

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* Extrinsic regulatory system that includes neural and humoral factors.

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* A discrepancy between tissue oxyegn demand and supply raises the concentration of local [[metabolites]] such as [[hydrogen]], [[potassium]], [[carbon dioxide]], and [[adenosine]], resulting in [[vasodilation]], and [[hyperemia]].

** Reduction in blood supply to the mesentery causes adaptive changes in the splanchnic circulation.

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* An [[acute]] decrease in [[perfusion pressure]] is compensated for by a reduction in arteriolar wall tension, thereby maintaining [[splanchnic]] blood flow.

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** A discrepancy between tissue oxyegn demand and supply raises the concentration of local metabolites such as hydrogen, potassium, carbon dioxide, and adenosine, resulting in vasodilation and hyperemia.

* Although numerous types of neural stimulation (e.g. [[vagal]], [[cholinergic]], histaminergic, and [[sympathetic]]) can affect the blood supply of the gut, the [[adrenergic]] limb of the [[autonomic nervous system]] is the predominant neural influence on [[splanchnic]] circulation.

** Intense activation of vasoconstrictor fibers through alpha-adrenergic stimulation results in vasoconstriction of small vessels and a decrease in mesenteric blood flow.

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** After periods of prolonged alpha-adrenergic vasoconstriction, blood flow increases, presumably through β-adrenergic stimulation, which acts as a protective response.

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** Although numerous types of neural stimulation (e.g. vagal, cholinergic, histaminergic, and sympathetic) can affect the blood supply of the gut, the adrenergic limb of the autonomic nervous system is the predominant neural influence on splanchnic circulation.

* Grade 3. There is [[congestion]] of mucosa with loss of superficial [[Gland|glandular]] architecture, but deep villous architecture is preserved.

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* Grade 4. [[Muscle|Muscular]] layer is preserved, but the mucosa is completely involved, with loss of all superficial and deep [[Gland|glandular]] architecture.

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* Grade 5. There is total loss of [[Gland|glandular]] architecture, and the muscularis propria shows degeneration, fragmentation, and [[Skeletal muscle|myocyte]] death, all of which indicate transmural [[infarction]].

In order to compensate for the ischemia, there is vasoconstriction of mesenteric vessels resulting in increased tissue oxygen extraction along with vasodilation of the collateral vessels. Owing to this mechanism, intestine is able to compensate for around 75% reduction in blood flow.[1][2][3][4][5][6]

Factors contributing in the pathogenesis of mesenteric ischemia:[7][8]